OBJECTIVE: To investigate the preventive effect of ulinastatin on shock in the heart after burn. METHODS: In an open prospective clinical study 34 adults with burns >50% total body surface area were randomly divided into control (B) and ulinastatin-treated (U) groups. All underwent routine treatment, and group U received 100,000U ulinastatin intravenously three times a day for 1 week. In an animal experiment, 72 healthy rats underwent equivalent burn, similar division into groups B and U, and resuscitation according to Parkland's formula. Rats in group U received ulinastatin (40,000U/kg) immediately after burn. Myocardial pathomorphology, plasma cTnI, CK-MB and PMNE, myocardial MDA, TNF-alpha, IL-10 and caspase-3 activity and cardiocyte apoptosis were determined. RESULTS:Plasma cTnI, CK-MB, and PMNE were higher in clinical group B than group U. In the animal experiment, plasma cTnI, CK-MB, myocardial MDA, TNF-alpha, IL-10 and caspase-3 activity, and apoptotic index and myocardial pathomorphological changes were significantly less in group U than in group B, save IL-10. CONCLUSION: The clinical and experimental data showed that ulinastatin relieved myocardial damage from severe burn. The mechanism might involve modulation of the anti- and pro-inflammatory balance and lipid peroxidation, and decreased myocardiocyte apoptosis.
RCT Entities:
OBJECTIVE: To investigate the preventive effect of ulinastatin on shock in the heart after burn. METHODS: In an open prospective clinical study 34 adults with burns >50% total body surface area were randomly divided into control (B) and ulinastatin-treated (U) groups. All underwent routine treatment, and group U received 100,000U ulinastatin intravenously three times a day for 1 week. In an animal experiment, 72 healthy rats underwent equivalent burn, similar division into groups B and U, and resuscitation according to Parkland's formula. Rats in group U received ulinastatin (40,000U/kg) immediately after burn. Myocardial pathomorphology, plasma cTnI, CK-MB and PMNE, myocardial MDA, TNF-alpha, IL-10 and caspase-3 activity and cardiocyte apoptosis were determined. RESULTS: Plasma cTnI, CK-MB, and PMNE were higher in clinical group B than group U. In the animal experiment, plasma cTnI, CK-MB, myocardial MDA, TNF-alpha, IL-10 and caspase-3 activity, and apoptotic index and myocardial pathomorphological changes were significantly less in group U than in group B, save IL-10. CONCLUSION: The clinical and experimental data showed that ulinastatin relieved myocardial damage from severe burn. The mechanism might involve modulation of the anti- and pro-inflammatory balance and lipid peroxidation, and decreased myocardiocyte apoptosis.